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Thalidomide is a sedative drug introduced to European markets on 1 October 1957 after extensive testing on rodent embryos to ensure its safety. Early laboratory tests in rodent populations showed that pregnant rodents could safely use it, so doctors prescribed Thalidomide to treat morning sickness in pregnant women. However, in humans Thalidomide interfered with embryonic and fetal development in ways not observed in rodent tests.

Maternal consumption of alcohol (ethanol) can result in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The eye and ocular system development is particularly susceptible to the effects of prenatal alcohol exposure and can result in visual impairment or blindness.

Angelman syndrome is a disorder in humans that causes neurological symptoms such as lack of speech, jerky movements, and insomnia. A human cell has two copies of twenty-three chromosomes for a total of forty-six-one copy from its mother and one from its father. But in the case of Angelman syndrome, the maternal chromosome numbered 15 has a mutation or deletion in its DNA and a gene on the paternal chromosome 15 is inactivated in some parts the brain. The result is the paternal gene is silenced during development of the sperm, which is called genetic imprinting.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) is part of this group and was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities and defects of the central nervous system (CNS). The CNS is particularly vulnerable to the effects of ethanol during prenatal development.

Prenatal exposure to alcohol (ethanol) in human and animal models results in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The basal ganglia, one of the central nervous system components, are affected by exposure to ethanol during development.

Prenatal exposure to alcohol (ethanol) can result in a continuum of developmental abnormalities that are highly variable depending on the severity, duration, frequency, and timing of exposure during gestation. Defects of the corpus callosum (CC) have proven to be a reliable indicator of prenatal alcohol exposure as it affects the brain. Structural abnormalities of the CC occur along a continuum, like most alcohol-induced anomalies, whereby more severe prenatal exposure results in a greater expression of the abnormal trait.

Methylmercury (MeHg) is an organic form of mercury that can damage the developing brains of human fetuses. Women who consume methylmercury during pregnancy can bear children who have neurological issues because methylmercury has toxic effects on the nervous system during embryonic development. During the third week of gestation, the human nervous system begins to form in the embryo. During this gestational period, the embryo's nervous system is particularly susceptible to the influence of neurotoxins like methylmercury that can result in abnormalities.

Mitochondrial diseases in humans result when the small organelles called mitochondria, which exist in all human cells, fail to function normally. The mitochondria contain their own mitochondrial DNA (mtDNA) separate from the cell's nuclear DNA (nDNA). The main function of mitochondria is to produce energy for the cell. They also function in a diverse set of mechanisms such as calcium hemostasis, cell signaling, regulation of programmed cell death (apoptosis), and biosynthesis of heme proteins that carry oxygen.

Many difficulties can arise with a pregnancy even after the sperm successfully fertilizes the oocyte. A major problem occurs if the fertilized egg tries to implant before reaching its normal implantation site, the uterus. An ectopic pregnancy occurs when a fertilized egg implants anywhere other than in the uterus, most commonly in the fallopian tubes. Ectopic pregnancies cannot continue to term, so a physician must remove the developing embryo as early as possible.

The concept Fetal Alcohol Syndrome (FAS) refers to a set of birth defects that occur in children born to mothers who abused alcohol during pregnancy. The alcohol-induced defects include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing central nervous system (CNS).

Maternal consumption of alcohol (ethanol) during pregnancy can result in a continuum of embryonic developmental abnormalities that vary depending on the severity, duration, and frequency of exposure of ethanol during gestation. Alcohol is a teratogen, an environmental agent that impacts the normal development of an embryo or fetus. In addition to dose-related concerns, factors such as maternal genetics and metabolism and the timing of alcohol exposure during prenatal development also impact alcohol-related birth defects.

Anencephaly is an open neural tube defect, meaning that part of the neural tube does not properly close or that it has reopened during early embryogenesis. An embryo with anencephaly develops without the top of the skull, but retains a partial skull, including the face. Anencephaly is one of the most common birth defects of the neural tube, occurring at a rate of approximately one in one thousand human pregnancies. The condition can be caused by environmental exposure to chemicals, dietary deficiencies, or genetic mutations.

The Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene was identified in 1989 by geneticist Lap-Chee Tsui and his research team as the gene associated with cystic fibrosis (CF). Tsui's research pinpointed the gene, some mutations to which cause CF, and it revealed the underlying disease mechanism. The CFTR gene encodes a protein in the cell membrane in epithelial tissues and affects multiple organ systems in the human body. Mutations in the CFTR gene cause dysfunctional regulation of cell electrolytes and water content.

In the US, one in 1000 births is affected by neural tube defects (NTD). A neural tube defect is a birth defect involving the malformation of body features associated with the brain and spinal cord. An NTD originates from and is characterized by incomplete closure of the neural tube, which is an organizer and precursor of the central nervous system.

Bisphenol A (BPA) is an organic compound that was first synthesized by Aleksandr Dianin, a Russian chemist from St. Petersburg, in 1891. The chemical nomenclature of BPA is 2,2-bis (4-hydroxyphenyl) propane. The significance of this synthesized compound did not receive much attention until 1936, when two biochemists interested in endocrinology, Edward Dodds and William Lawson, discovered its ability to act as an estrogen agonist in ovariectomized, estrogen-deficient rats.

Estrogen plays a key role in the regulation of gene transcription. This is accomplished by its ability to act as a ligand and to bind to specific estrogen receptor (ER) molecules, such as ERα and ERβ, which act as nuclear transcription factors. There are three major nuclear estrogen receptor protein domains: the estrogen binding domain, the protein interaction domain, and the DNA binding domain.

Embryogenesis is an intricate process that can easily be disrupted by means of teratogenic agents. Some of these agents target the embryonic period's "window of susceptibility," three to eight weeks after a pregnant woman's last menstruation, when the highest degree of sensitivity to embryonic cell differentiation and organ formation occurs. The embryonic period or critical period is when most organ systems form, whereas the fetal period, week eight to birth, involves the growth and modeling of the organ systems.

Rh incompatibility occurs when a pregnant woman whose blood type is Rh-negative is exposed to Rh-positive blood from her fetus, leading to the mother s development of Rh antibodies. These antibodies have the potential to cross the placenta and attach to fetal red blood cells, resulting in hemolysis, or destruction of the fetus 's red blood cells. This causes the fetus to become anemic, which can lead to hemolytic disease of the newborn. In severe cases, an intrauterine blood transfusion for the fetus may be required to correct the anemia.

In 1914 Albert Niemann, a German pediatrician who primarily studied infant metabolism, published a description of an Ashkenazi Jewish infant with jaundice, nervous system and brain impairments, swollen lymph nodes (lymphadenopathy), and an enlarged liver and spleen (hepatosplenomegaly). He reported that these anatomical disturbances resulted in the premature death of the child at the age of eighteen months. After extensively studying the abnormal characteristics of the infant, Niemann came to the conclusion that the disease was a variant of Gaucher's disease.

Teratogens are substances that may produce physical or functional defects in the human embryo or fetus after the pregnant woman is exposed to the substance. Alcohol and cocaine are examples of such substances. Exposure to the teratogen affects the fetus or embryo in a variety of ways, such as the duration of exposure, the amount of teratogenic substance, and the stage of development the embryo or fetus is in during the exposure.

John Hilton Edwards first described the symptoms of the genetic disorder known as Trisomy 18 - one of the most common forms of trisomy, which occurs when cells have an extra copy of a chromosome, in humans - in 1960. Trisomy 18, also known as Edwards Syndrome, occurs approximately once per 6000 live births and is second in frequency only to Trisomy 21, or Down's Syndrome, as an autosomal trisomy. Trisomy 18 causes substantial developmental problems in utero.

A variety of developmental defects occur as a result of prenatal exposure to alcohol (ethanol) in utero. In humans, those defects are collectively classified as Fetal Alcohol Spectrum Disorders, with Fetal Alcohol Syndrome (FAS) representing the more severe defects. FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). In addition to those defects, prenatal exposure to alcohol impacts cardiogenesis, the developmental stage of heart formation.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading Fetal Alcohol Spectrum Disorder (FASD). Fetal Alcohol Syndrome (FAS) was first defined in 1973 as a condition characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system. The pattern of facial defects that occur as a result of ethanol exposure during development primarily affects the midline of the face, altering morphology of the eyes, nose, and lips.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system (CNS).

Parasitic twins, a specific type of conjoined twins, occurs when one twin ceases development during gestation and becomes vestigial to the fully formed dominant twin, called the autositic twin. The underdeveloped twin is called parasitic because it is only partially formed, is not functional, or is wholly dependent on the autositic twin.